Canine Distemper |Symptoms of Distemper Virus in Dogs| Treatment of Canine Distemper|

 


Canine Distemper (Distemper: Out of order, Dysfunctional)

Synonymous

Hard pad disease, Canine plague. The virus was first isolated in the USA in 1905

Etiology:

CD Virus, Genus Morbili virus, Family Paramyxoviridae

The disease was first discovered in 1950 in South Africa, in 1983 in the USA.

Size of virus:

Variable size, 150-250nm. Single negative-strand RNA virus.

Negative sense RNA: Whose sequence is complementary to mRNA. Therefore it is first converted to Positive sense RNA before transcription.

More than 20 strains and each strain has different pathogenicity. The virus can survive at low temperatures 0-4C (survives for 7 days at this temperature). At 50-60C, it is capable to survive up to 30 minutes. Humidity and low temperature increase its survival. At -65C it can survive up to 7 years. At 37C it can survive up to 3 days.

pH

4.5-9 is more viable. Less than or more than this pH will result in less survival of the virus.

0.3% carbolic acid can be used to destroy it.

Host range:

Ø  Canidae

Ø  Felidae

Ø  Pandas

Ø  Ferrets

Ø  ……..

Epidemiology:

Present throughout the world. Prevalence is more in Asia, controlled in the USA.

Transmission:

From infected animals to healthy animals is through aerosol, secretions, shedding (7 days), shedding in urine also. The virus could be secreted up to 60-70 days post-infection. Also transplacental transmission.

Built-in CD virus in Newborn puppies. Signs appear in them at the age of 4-6 weeks. From the dam to puppies. Animal remains carrier throughout its life and this is the major reason that disease cannot be controlled.

Contact of diseased or carrier animal. Recovered animal gets lifelong immunity.

Vaccination:

Through vaccination, immunity is not lifelong. The immunized animal will develop signs and symptoms when the contact with diseased or carrier animal occurs.

25-75% of the canine population is infected from CD virus and become carriers throughout life.  (Virus resides in CNS)

Age:

In cosmopolitan dogs 3-6 months

Isolated dogs: can be affected at any age. Severity is much greater than cosmopolitan.

Brachiocephalic animals (Flat and wide skull shape):

Severity and prevalence are less.

Dolichocephalic dogs (Having a narrow and long head):

More severity and prevalence. Fewer chances of survival.

Mesaticephalic dogs (A skull with the cranium and nasal cavity about equal lengths)

Strains:

1)      Synder hill ( causes polioencephalomalacia )

2)      A 75/17

3)      R2 S2

These all strains are highly virulent. Fewer chances of survival.

Pathogenesis:

Systemic infection

It gains entry through aerosol. So 1st it resides in the epithelium of URT. Up to 24 hours, it multiplies there. Then it is transferred to tonsils, bronchial and retropharyngeal lymph nodes. Multiplies in these organs up to 2-4 days post-infection. Viremia develops which is transferred to the spleen, lamina propria of the stomach and small intestine, mesenteric lymph nodes, kupffer cells of the liver. Multiplication in these organs occurs after 4 days post-infection.

After 6 days post-infection, fiver, leukopenia (primarily lymphopenia). Then shedding of the virus starts.

9-14 days post infection:

1)    Strong immune system

If the strong immune system, it will clear the virus from the body of an animal. This animal will not be the carrier of virus.

2)    Intermediate immune system

The virus multiplies in the spleen, stomach, small intestine, liver and spreads to CNS and the integumentary system. After the virus has reached to CNS, the animal will become carriers of the virus. The animal may or may not show the signs of disease but it is a carrier of the CD virus.

3)    Weak immune system

Severe signs of disease. More chances of death. The virus spreads to all body systems.

CNS infections

After entry in CNS, Virus maybe free or lymphocyte-associated, 3 target sites in CNS:

i)                    Perivascular of meninges

ii)                  Choroid plexus of 4th ventricle

iii)                Ependymal structures ( cells of ventricles )

The most productive of these is the choroid plexus i.e. it spreads the virus further to

i)                    Spinal cord

ii)                  Cerebral structures

iii)                Subpial

iv)                CSF

Factors which prevent further spread of the virus:

i)                    Age of animal

ii)                  Immune status

iii)                How much neurotropic is the strain of virus

Clinical signs

There is variation in clinical signs

Ø  Systemic signs

Ø  Neurologic signs

Ø  Neonatal signs

Ø  Bone lesions

Ø  Ocular signs

Systemic signs

Depend upon

Ø  Virulence of strain

Ø  Environmental condition

Ø  Age of the animal

Ø  Immune system

Signs are:

i)                    Fiver (104-106F)

ii)                  Dullness

iii)                Anorexia

iv)                Depression

v)                  Mucopurulent discharge from nostril

vi)                Dry cough and then convert to productive cough

vii)              Keratoconjuctivitis

viii)            Persistent anosmia

ix)                More lower respiratory sounds ( through auscultation )

x)                  Vomiting un related to eating

xi)                Diarrhea (shooting). Could be blood-tinged. Could have mucus in it.

xii)              Dehydration

xiii)            Academia

xiv)            Tenesmus

xv)              Sudden death

Neurological signs

These signs can occur simultaneously with systemic infection but this case is rare. Mostly neurological signs occur 1-3 weeks after recovering from systemic infection.

Nervous signs are always progressive

These signs define mortality

These signs include:

i)                    Hyperesthesia

ii)                  Par paresis

iii)                Tetra paresis

iv)                Chewing gum reflexes

v)                  Seizures

vi)                Champing of jaws

vii)              Chorea

viii)            Myoclonus (involuntary twitching of muscles) or involuntary movement of any body part.

ix)                Paralysis of forelimbs associated with myoclonus

x)                  Ataxia

xi)                Cervical stiffness

These signs are more rhythmic while the animal is sleeping.

Trans placental infections:

If the dam survives from CD, following signs may occur

Ø  Stillbirth ( dystocia )

Ø  Abortion

If puppies are born alive, signs of CD will appear at the age of 4-6 weeks. Mostly neurological signs appear in them.

Neonatal infections: (Neonate: fetus of 1st 28 days)

Signs in neonates include:

i)                    Week dentin

ii)                  Enamel hypoplasia

iii)                Bone lesions

iv)                Metaphyseal osteosclerosis of long bones ( hardening of bone in the metaphyseal region )

v)                  Keratoconjunctivitis which may lead to blindness

Treatment

No specific treatment. Supportive treatment is done to increase the chances of survival.

Prevention and control

Ø  Vaccination is the foremost preventive measure

Ø  3-4 weeks of age------------ 1st shot of CD

Ø  Again another shot after 3-4 weeks

Ø  Also 3rd time

Ø  If the disease is prevalent in the area, then the duration between shots should be less (2-3 weeks)

Ø  Isolate the infected animal and clean the Kennel with any disinfectant

Ø  No zoonotic risk

 

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